scholarly journals Hepatic SIRT3 Upregulation in Response to Chronic Alcohol Consumption Contributes to Alcoholic Liver Disease in Mice

2019 ◽  
Vol 10 ◽  
Author(s):  
Yue Ma ◽  
Hui Chai ◽  
Qinchao Ding ◽  
Qianyu Qian ◽  
Zhaoyuan Yan ◽  
...  
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Alcoholic Liver Disease ◽  
Chronic Alcohol ◽  
Chronic Alcohol Consumption

scholarly journals Regulatory T cells suppress excessive lipid accumulation in alcoholic liver disease

2019 ◽  
Vol 60 (5) ◽  
pp. 922-936 ◽  
Author(s):  
Hongwu Wang ◽  
Ting Wu ◽  
Yaqi Wang ◽  
Xiaoyang Wan ◽  
Junying Qi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
Liver Disease ◽  
Alcohol Consumption ◽  
Regulatory T Cells ◽  
Alcoholic Liver Disease ◽  
Lipid Accumulation ◽  
Chronic Alcohol ◽  
Chronic Alcohol Consumption ◽  
Alcoholic Fatty Liver

Sensitization of hepatic immune cells from chronic alcohol consumption gives rise to inflammatory accumulation, which is considered a leading cause of liver damage. Regulatory T cells (Tregs) are an immunosuppressive cell subset that plays an important role in a variety of liver diseases; however, data about pathological involvement of Tregs in liver steatosis of alcoholic liver disease (ALD) is insufficient. In mouse models of ALD, we found that increased lipid accumulation by chronic alcohol intake was accompanied by oxidative stress, inflammatory accumulation, and Treg decline in the liver. Adoptive transfer of Tregs relieved lipid metabolic disorder, oxidative stress, inflammation, and, consequently, ameliorated the alcoholic fatty liver. Macrophages are a dominant source of inflammation in ALD. Aberrant macrophage activation and cytokine production were activated during chronic alcohol consumption, but were significantly inhibited after Treg transfer. In vitro, macrophages were co-activated by alcohol and lipopolysaccharide to mimic a condition for alcoholic liver microenvironment. Tregs suppressed monocyte chemoattractant protein-1 and TNF-α production from these macrophages. However, such effects of Tregs were remarkably neutralized when interleukin (IL)-10 was blocked. Altogether, our data uncover a novel role of Tregs in restoring liver lipid metabolism in ALD, which partially relies on IL-10-mediated suppression of hepatic pro-inflammatory macrophages.

scholarly journals Study of clinical and biochemical profile of acute alcoholic liver disease in a teaching hospital in Telangana

2018 ◽  
Vol 5 (4) ◽  
pp. 804
Author(s):  
Shamsunder Khatroth
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Alcoholic Liver Disease ◽  
Biochemical Parameters ◽  
Clinical Manifestations ◽  
Age Group ◽  
Biochemical Profile ◽  
Chronic Alcohol ◽  
Chronic Alcohol Consumption ◽  
Female Ratio

Background: Chronic alcohol consumption gives rise to various health risks that include liver disease, heart disease, pancreatitis, central nervous system disorders and certain forms of cancer. Alcoholic liver disease (ALD) is a spectrum of clinicopathological abnormalities, reflecting an acute or chronic inflammation of the liver parenchyma induced by alcohol use. It is associated with changes in various biochemical parameters and also various clinical manifestations in the patients. The objective of the present study to evaluate clinical and biochemical profile of acute alcoholic liver disease.Methods: The prospective hospital-based case control study was done at MNR Medical College, in the department of General Medicine for duration of one year from March 2017 to April 2018. A total of 120 cases diagnosed clinically and biochemically as Acute alcoholic liver disease were included in the study.Results: The age group ranged from 20 to 60 years and the male to female ratio was 2.42. Majority of the patients were in the age group of 30-40 years (54.1%).  Majority of the patients (66.6%) consumed >60 grams/24hours of alcohol. Jaundice, nausea and vomiting were seen in 83.3% cases followed by hepatomegaly in 66.6% cases. Majority of them had been consuming alcohol for more than 5 years.Conclusions: Chronic alcohol consumption is more common in adult males. Chronic alcoholics consume more amount of alcohol. Alcoholic liver disease has a varied clinical presentation and is associated with deranged biochemical parameters.

scholarly journals Alcohol induced hepatic retinoid depletion is associated with the induction of multiple retinoid catabolizing cytochrome P450 enzymes

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0261675
Author(s):  
Afroza Ferdouse ◽  
Rishi R. Agrawal ◽  
Madeleine A. Gao ◽  
Hongfeng Jiang ◽  
William S. Blaner ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Retinoic Acid ◽  
Liver Disease ◽  
Alcohol Consumption ◽  
Vitamin A ◽  
Alcohol Exposure ◽  
Chronic Alcohol ◽  
Wild Type ◽  
Chronic Alcohol Consumption ◽  
Retinyl Esters

Chronic alcohol consumption leads to a spectrum of liver disease that is associated with significant global mortality and morbidity. Alcohol is known to deplete hepatic vitamin A content, which has been linked to the pathogenesis of alcoholic liver disease. It has been suggested that induction of Cytochrome P450 2E1 (CYP2E1) contributes to alcohol-induced hepatic vitamin A depletion, but the possible contributions of other retinoid-catabolizing CYPs have not been well studied. The main objective of this study was to better understand alcohol-induced hepatic vitamin A depletion and test the hypothesis that alcohol-induced depletion of hepatic vitamin A is due to CYP-mediated oxidative catabolism. This hypothesis was tested in a mouse model of chronic alcohol consumption, including wild type and Cyp2e1 -/- mice. Our results show that chronic alcohol consumption is associated with decreased levels of hepatic retinol, retinyl esters, and retinoic acid. Moreover, the depletion of hepatic retinoid is associated with the induction of multiple retinoid catabolizing CYPs, including CYP26A1, and CYP26B1 in alcohol fed wild type mice. In Cyp2e1 -/- mice, alcohol-induced retinol decline is blunted but retinyl esters undergo a change in their acyl composition and decline upon alcohol exposure like WT mice. In conclusion, the alcohol induced decline in hepatic vitamin A content is associated with increased expression of multiple retinoid-catabolizing CYPs, including the retinoic acid specific hydroxylases CYP26A1 and CYP26B1.

Alcohol consumption patterns in heavy drinkers with and without alcoholic liver disease (ALD)

2001 ◽  
Vol 120 (5) ◽  
pp. A117-A117
Author(s):  
K DEAR ◽  
M BRADLEY ◽  
K MCCORMACK ◽  
R PECK ◽  
D GLEESON
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Alcoholic Liver Disease ◽  
Consumption Patterns ◽  
Heavy Drinkers

Urinary ethyl glucuronide testing detects alcohol consumption in alcoholic liver disease patients awaiting liver transplantation

2007 ◽  
Vol 13 (5) ◽  
pp. 757-761 ◽  
Author(s):  
Yesim Erim ◽  
Michael Böttcher ◽  
Uta Dahmen ◽  
Olof Beck ◽  
Christoph E. Broelsch ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Liver Disease ◽  
Alcohol Consumption ◽  
Alcoholic Liver Disease ◽  
Ethyl Glucuronide

scholarly journals Chronic Alcohol Consumption Leads to a Tissue Specific Expression of Uncoupling Protein-2

2015 ◽  
Vol 12 (12) ◽  
pp. 995-999 ◽  
Author(s):  
Jan A. Graw ◽  
Clarissa von Haefen ◽  
Deniz Poyraz ◽  
Nadine Möbius ◽  
Marco Sifringer ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Chronic Alcohol ◽  
Specific Expression ◽  
Chronic Alcohol Consumption ◽  
Tissue Specific ◽  
Tissue Specific Expression

Decreased Hepatotoxicity of Dimethylnitrosamine (DMN) Following Chronic Alcohol Consumption

1980 ◽  
pp. 237-243
Author(s):  
J. Gellert ◽  
F. Moreno ◽  
M. Haydn ◽  
H. Oldiges ◽  
H. Frenzel ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Chronic Alcohol ◽  
Chronic Alcohol Consumption

scholarly journals Genetic and Epigenetic Modifiers of Alcoholic Liver Disease

2018 ◽  
Vol 19 (12) ◽  
pp. 3857 ◽  
Author(s):  
Marica Meroni ◽  
Miriam Longo ◽  
Raffaela Rametta ◽  
Paola Dongiovanni
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Alcoholic Liver Disease ◽  
Complex Disease ◽  
Wide Spectrum ◽  
Association Studies ◽  
Phenotypic Variability ◽  
Genome Wide Association Studies ◽  
Epigenetic Factors ◽  
Excessive Alcohol Consumption

Alcoholic liver disease (ALD), a disorder caused by excessive alcohol consumption is a global health issue. More than two billion people consume alcohol in the world and about 75 million are classified as having alcohol disorders. ALD embraces a wide spectrum of hepatic lesions including steatosis, alcoholic steatohepatitis (ASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). ALD is a complex disease where environmental, genetic, and epigenetic factors contribute to its pathogenesis and progression. The severity of alcohol-induced liver disease depends on the amount, method of usage and duration of alcohol consumption as well as on age, gender, presence of obesity, and genetic susceptibility. Genome-wide association studies and candidate gene studies have identified genetic modifiers of ALD that can be exploited as non-invasive biomarkers, but which do not completely explain the phenotypic variability. Indeed, ALD development and progression is also modulated by epigenetic factors. The premise of this review is to discuss the role of genetic variants and epigenetic modifications, with particular attention being paid to microRNAs, as pathogenic markers, risk predictors, and therapeutic targets in ALD.

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